14 - Ischaemia, infarction and shock Flashcards

1
Q

Why is reperfusion of non-infarcted but ischaemic tissues not always good?

A

Generation of reactive oxygen species by inflammatory cells causes further cell damage === reperfusion injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Main causes of infarctions

A

Thrombosis and embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Other causes of infarctions

A
vasopasm
artheroma expansion
extrinsic compression
twisting of vessel roots (volvulus)
rupture of vascular supply (AAA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Infarction morphology

A

Red (haemorrhagic)

White (anaemic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what necrosis in the brain

A

colliquative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

most popular necrosis

A

coagulative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

if someone dies of a sudden heart attack what histology do you see?

A

nothing! as no time to develop haemorrhage / inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

factors affecting the degree of ischaemic damage

A

nature of the blood supply
rate of occlusion
tissue vulnerability to hypoxia
blood o2 content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

most vulnerable organs for infarction

A

kidneys, spleen, testis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

a slow rate of occlusion makes you more or less likely to have an infarct?

A

less likely as it allows development of collateral perfusion pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

blood oxygen content

A

anaemia increases chance of infarction

congestive heart failure - poor CO and impaired pulm. vent. may develop an infarct with normally inconsequential narrowing of the vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

shock definition

A

physiological state characterised by significant reduction of systemic tissue perfusion (severe hypotension) resulting in decreased O2 delivery to the tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

shock’s effects at a cellular level

A

Membrane ion pump dysfunction
Intracellular swelling
Leakage of intracellular contents into the extracellular space
Inadequate regulation of intracellular pH
Anaerobic resp –> lactic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

shock’s effects at a systemic level

A

Alterations in the serum pH (acidaemia)
Endothelial dysfunction -> vascular leakage
Stimulation of inflammatory and anti-inflammatory cascades
End-organ damage (ischaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Shock and reversibility

A

Shock is initially reversible but rapidly becomes irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Result of shock

A

Cell death
End-organ damage
Multi-organ failure
Death

17
Q

Classification of shock

A

Hypovolaemic
Cardiogenic
Distributive

18
Q

Types of distributive shock

A

Anaphylactic
Septic
Toxic shock syndrome
Neurogenic

19
Q

Hypovolaemic shock

A

Intra-vascular fluid loss (blood, plasma etc)
Decrease in venous return to heart aka pre-load
Lower stroke volume therefore low CO

20
Q

How to compensate for hypovolaemic shock

A

Increase blood volume

21
Q

Causes of hypovolaemic shock

A

Haemorrhage - trauma, GI, rupture, fractures, aneurysm rupture

Non-haemorrhagic - diarrhoea, vomiting, heat stroke, burns

Third spacing

22
Q

What is third spacing?

A

Acute loss of fluid into internal body cavities

Third-space losses are common post-op and in GI obstruction, pancreatitis or cirrhosis

23
Q

Cardiogenic shock - why? how to compensate?

A

Cardiac pump failure with low CO

How to compensate -> increase in systemic vascular resistance

24
Q

Causes of cardiogenic shock

A

Myopathic (heart muscle failure)
Arrythmia related
Mechanical
Extra cardiac (obstruction to blood flow)

25
Extra cardiac cardiogenic shock e.g.s
Anything that impairs cardiac filling or ejection of blood from heart Massive PE, tension PT, severe constrictive pericarditis, pericardial tamponade
26
Distributive shock
Decrease in systemic vascular resistance due to severe vasodilation Compensate via increasing CO
27
Septic shock which organisms? who's at risk? pathophysiogical features
Gram +ve, -ve bacteria or fungi and affects immunocompromised, elderly, very young Increase in cytokines/mediators leading to vasodilation Pro-coagulation (DIC)
28
Anaphylactic shock - pathophysiology
Severe type I hypersensitivity rxn Small doses of allergen = IgE cross-linking Massive mast cell degranulation which = vasodilation
29
Anaphylactic shock - body's rxn
Contraction of bronchioles/ resp. distress Laryngeal oedema Circulatory collapse -> shock/death
30
Neurogenic shock
Spinal injury / anaesthetic accidents = loss of sympathetic vascular tone Vasodilation -> shock
31
Toxic shock syndrome
NOT SAME AS SEPTIC SHOCK
32
Toxic shock syndrome - causative organism
S. aureus | S. pyogenes
33
Toxic shock syndrome - pathophysiology
do not require processing by APCs non-specific binding of MHC II to T cell receptors with up to 20% of T cells being activated at once Widespread cytokine release = decrease in SVR